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Holsen, Laura

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Holsen

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Laura

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Holsen, Laura
Author's Publications: search.filters.isAuthorOfPublication.57850e4b-db9a-438c-8bf7-b80dc062a4f5

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    Reverse-Translational Identification of a Cerebellar Satiation Network
    (Springer Science and Business Media LLC, 2021-11-17) Low, Aloysius Y. T.; Goldstein, Nitsan; Gaunt, Jessica R.; Huang, Kuei-Pin; Zainolabidin, Norliyana; Yip, Alaric K. K.; Carty, Jamie R. E.; Choi, Ju Y.; Miller, Alekso M.; Ho, Helen S. T.; Lenherr, Clara; Baltar, Nicholas; Abdel-Azim, Eiman; Sessions, October M.; Ch’ng, Toh Hean; Bruce, Amanda S.; Martin, Laura E.; Halko, Mark; Brady, Roscoe O. Jr; Holsen, Laura; Alhadeff, Amber L.; Chen, Albert I.; Betley, J. Nicholas
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    Reward Capacity Predicts Leptin Dynamics During Laboratory-Controlled Eating in Women as a Function of Body Mass Index
    (2017) Holsen, Laura; Jackson, Benita
    Objective: The role of leptin in mesolimbic signaling non-food-related reward has been well established at the pre-clinical level, yet studies in humans are lacking. The present investigation explored the association between hedonic capacity and leptin dynamics, and whether this association differed by BMI class. Methods: In this cross-sectional study of 75 women (42 with lean BMIs, 33 with obese BMIs), we measured serum leptin before/after meal consumption. Reward capacity was assessed using the Snaith-Hamilton Pleasure Scale (SHAPS). Multiple regression tested whether reward capacity was associated with leptin AUC, with an interaction term to test differences between lean (LN) and obese (OB) groups. Results: The interaction of SHAPS by BMI group was robust (β=−.40, p=.005); among women with obesity, greater SHAPS score was associated with lower leptin AUC (β=−.35, p=.002, adjusted R-squared=.66). Among the lean group, the association was not statistically significant (β=−.16, p=.252, adjusted R-squared=.22). Findings were above and beyond BMI and age. Conclusions: In this sample a robust, negative association between reward capacity and circulating leptin was stronger in women with obesity compared to lean counterparts. These findings suggest that despite likely leptin resistance, inhibitory leptin functioning related to non-food reward may be spared in women with obesity.
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    Fetal hormonal programming of sex differences in depression: linking women's mental health with sex differences in the brain across the lifespan
    (Frontiers Media S.A., 2014) Goldstein, Jill; Holsen, Laura; Handa, Robert; Tobet, Stuart
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    Importance of Reward and Prefrontal Circuitry in Hunger and Satiety: Prader-Willi Syndrome vs. Simple Obesity
    (2011) Holsen, Laura; Savage, Cary R.; Martin, Laura E.; Bruce, Amanda S.; Lepping, Rebecca J.; Ko, Eunice; Brooks, William M.; Butler, Merlin G.; Zarcone, Jennifer R.; Goldstein, Jill
    Background: The majority of research on obesity has focused primarily on clinical features (eating behavior, adiposity measures), or peripheral appetite-regulatory peptides (leptin, ghrelin). However, recent functional neuroimaging studies have demonstrated that some reward circuitry regions which are associated with appetite-regulatory hormones are also involved in the development and maintenance of obesity. Prader-Willi syndrome (PWS), characterized by hyperphagia and hyperghrelinemia reflecting multi-system dysfunction in inhibitory and satiety mechanisms, serves as an extreme model of genetic obesity. Simple (non-PWS) obesity (OB) represents an obesity control state. Objective: This study investigated subcortical food motivation circuitry and prefrontal inhibitory circuitry functioning in response to food stimuli before and after eating in individuals with PWS compared with OB. We hypothesized that groups would differ in limbic regions (i.e., hypothalamus, amygdala) and prefrontal regions associated with cognitive control [i.e., dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC)] after eating. Design and Participants: Fourteen individuals with PWS, 14 BMI- and age-matched individuals with OB, and 15 age-matched healthy-weight controls (HWC) viewed food and non-food images while undergoing functional MRI before (pre-meal) and after (post-meal) eating. Using SPM8, group contrasts were tested for hypothesized regions: hypothalamus, nucleus accumbens (NAc), amygdala, hippocampus, OFC, medial PFC, and DLPFC. Results: Compared with OB and HWC, PWS demonstrated higher activity in reward/limbic regions (NAc, amygdala) and lower activity in hypothalamus and hippocampus, in response to food (vs. non-food) images pre-meal. Post-meal, PWS exhibited higher subcortical activation (hypothalamus, amygdala, hippocampus) compared to OB and HWC. OB showed significantly higher activity versus PWS and HWC in cortical regions (DLPFC, OFC) associated with inhibitory control. Conclusion: In PWS compared with obesity per se, results suggest hyperactivations in subcortical reward circuitry and hypoactivations in cortical inhibitory regions after eating, which provides evidence of neural substrates associated with variable abnormal food motivation phenotypes in PWS and simple obesity.